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El diálogo cruzado entre las enzimas modificadoras de lisina controla las amplificaciones de ADN específicas del
Sweta Mishra1, Capucine Van Rechem1, Sangita Pal1
1Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Cell
|July 31, 2018
Resumen
Los reguladores de la cromatina controlan el aumento del número de copias de ADN en los tumores. Las vías específicas de metilación H3K4 y una red distinta que involucra a KDM4B y KDM5B regulan las amplificaciones de ADN específicas del sitio.
Área de la Ciencia:
- La epigenética
- Biología del cáncer
- La genómica
Sus antecedentes:
- Las amplificaciones de ADN cromosómico adquiridas son características de numerosos cánceres.
- Si bien se conoce el papel de KDM4A en las ganancias transitorias de número de copias específicas del sitio (TSSGs), otros mecanismos que impulsan estas ganancias siguen sin estar claros.
Objetivo del estudio:
- Identificar nuevos reguladores de la cromatina involucrados en el control de las ganancias de copia de ADN específicas del sitio.
- Aclarar los mecanismos mediante los cuales los estados de metilación H3K4 y los reguladores asociados orquestan los TSSG.
Principales métodos:
- Investigó la función de los reguladores de la cromatina modificadores de H3K4 junto con los reguladores de H3K9/H3K36.
- Analizó las funciones de las metiltransferasas KDM5A, COMPASS/KMT2 y la red MLL1-KDM4B-KDM5B en la modulación del número de copias del ADN.
Principales resultados:
- Se descubrió que los reguladores de la cromatina modificadores de H3K4 cooperan con los reguladores de H3K9 / H3K36 para orquestar TSSGs.
- Se ha demostrado que las metiltransferasas KDM5A y COMPASS/KMT2 influyen en los loci TSSG a través de la metilación de H3K4 y el reclutamiento de KDM4A.
- Se identificó una vía independiente de KDM4A (MLL1-KDM4B-KDM5B) que regula el número de copias en un lugar específico.
Conclusiones:
- Estos hallazgos revelan un sistema de direccionamiento epigenético que rige la replicación y las amplificaciones de ADN específicas del sitio.
- El estudio destaca la compleja interacción de los modificadores de cromatina en la conducción de alteraciones del número de copias de ADN asociadas al tumor.
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